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In mature adults, glycine is a inhibitory neurotransmitter found in the spinal cord and regions of the brain. [15] As it binds to a glycine receptor, a conformational change is induced, and the channel created by the receptor opens. [17] As the channel opens, chloride ions are able to flow into the cell which results in hyperpolarization.
Sodium- and chloride-dependent glycine transporter 2, also known as glycine transporter 2 (GlyT2), is a protein that in humans is encoded by the SLC6A5 gene. [ 5 ] The glycine transporter 2 is a membrane protein which recaptures glycine , a major inhibitory transmitter in the spinal cord and brainstem .
Glycine transporters (GlyTs) are plasmalemmal neurotransmitter transporters. They serve to terminate the signaling of glycine by mediating its reuptake from the synaptic cleft back into the presynaptic neurons. There are two glycine transporters: glycine transporter 1 (GlyT1) and glycine transporter 2 (GlyT2). [1]
Glycine is degraded via three pathways. The predominant pathway in animals and plants is the reverse of the glycine synthase pathway mentioned above. In this context, the enzyme system involved is usually called the glycine cleavage system: [36] Glycine + tetrahydrofolate + NAD + ⇌ CO 2 + NH + 4 + N 5,N 10-methylene tetrahydrofolate + NADH + H +
Neurotransmitter transporters frequently use electrochemical gradients that exist across cell membranes to carry out their work. For example, some transporters use energy obtained by the cotransport, or symport, of Na + in order to move glutamate across membranes. Such neurotransporter cotransport systems are highly diverse, as recent ...
Golgi cells predominantly use GABA and glycine as neurotransmitters, although depending on their target, a single Golgi cell will selectively facilitate GABAergic or glycinergic transmission. When Golgi cells are activated, granule cells and UBCs exhibit GABAergic and glycinergic currents, respectively.
Elevation of extracellular synaptic glycine concentration by blockade of GlyT1 has been hypothesized to potentiate NMDA receptor function in vivo and to represent a rational approach for the treatment of schizophrenia and cognitive disorders. Several drug candidates have reached clinical trials.
Some neurons can release at least two neurotransmitters at the same time, the other being a cotransmitter, in order to provide the stabilizing negative feedback required for meaningful encoding, in the absence of inhibitory interneurons. [18] Examples include: GABA–glycine co-release. Dopamine–glutamate co-release.